The Role of Reactive oxygen species in Macrophage-Mediated Immune Response Against Mycobacterium tuberculosis - PubMed
7 hours ago
- #Mycobacterium tuberculosis
- #Reactive oxygen species
- #Macrophage immunity
- Mycobacterium tuberculosis (Mtb) is the primary pathogen causing tuberculosis in humans.
- Macrophages use reactive oxygen species (ROS) as a key defense mechanism against Mtb.
- The interaction between Mtb, macrophages, and ROS forms a complex, underexplored network.
- Cytoplasmic NADPH oxidase (NOX) and mitochondria in macrophages are major ROS sources.
- ROS activate signaling pathways like NF-κB, MAPK family, and Nrf2.
- ROS maintain macrophage activation and M1 polarization via metabolic reprogramming.
- ROS are involved in activating autophagy and apoptosis pathways in macrophages.
- Mtb evades immune responses by manipulating oxidative stress and macrophage death pathways.
- Mtb uses antioxidant enzymes like KatG to resist ROS-mediated killing.
- Virulent Mtb strains suppress macrophage apoptosis to survive and replicate.
- Future therapeutic strategies may involve modulating the Mtb-macrophage-ROS network.
- Clinical trials on antioxidants for TB treatment are limited and exploratory.